- Email: [email protected]
PAINLESS LITHOTRIPSY
650 AIRWAY MANAGEMENT DURING CARDIOPULMONARY RESUSCITATION
SiR,—Your Feb 6th editorial emphasised the importance of
cardiopulmonary
resuscitation
training and retraining for hospital
staff. However, I agree with Dr Lawler and his colleagues (Feb 27, p 468) that the aim of all hospital doctors being able to intubate is logistically impossible. Semi-skilled intubation by the occasional practitioner in difficult conditions is, all too often, counterproductive, because it takes too long and may result in unrecognised oesophageal placement. As such it is an inappropriate method of immediate airway management. Unfortunately Lawler and colleagues’ further suggestion that the technical aspects of advanced arrest management, including intubation, should be delegated to suitably trained paramedical staff does not address the major problem of such immediate management. There is no reason to assume that a paramedical team will arrive any sooner than current arrest teams. Therefore all staff must be adequately trained in simple and effective airway management. Who actually intubates is unimportant provided they well trained, rapid, and skilful. An effective, simple, and hygienic technique for one-person ventilation is mouth-to-mask, preferably with supplemental oxygen. This method is easily learned and retained, and should be taught in preference to a bag-valve-mask technique, which is a difficult method for one person to master and should therefore be taught as the more effective two-person technique.2 Cricoid pressure is an important adjunct to these methods and should receive more emphasis. Intubation training and retraining should be provided for senior members of the cardiac arrest team and of the intensive care unit and for designated accident and emergency are
personnel.
Semiautomatic defibrillators may be helpful. Intubation requires repeated practice, which, for the training of large numbers, cannot and should not be on patients. We find mannikins to be essential for such training. We, like others, have found that the use of mannikins for full simulated cardiac arrests and intubation induces anxiety, and junior doctors feel that these simulations help them to cope better with true cardiac arrest, allowing them to concentrate on difficulties. Thus the "sheer terror of intubating a cyanosed patient whose mouth is full of secretions" is replaced, with practice, by the ability to see such a patient as one with a major complication to be approached calmly and efficiently using well-rehearsed techniques. We agree that for the apnoeic patient the ideal is for rapid, skilled intubation. Where such skills are not available pocket masks with exhaled air ventilation and supplemental oxygen are superior to incompetent intubation attempts, inadequate "ambu" bagging, Brook airway, or exhaled air ventilation alone.’ Training in the use of pocket masks can be easily incorporated into a hospital’s basic life-support training programme. The answer to the question "CPR: whose job?" is that CPR remains a team response. Hospitals must ensure that there are enough defibrillators to permit the response to an arrest call to be rapid, and we should start to standardise the equipment provided. Someone able to defibrillate must be on the spot. An appropriate protocol for airway management should be arrived at.’ Those who respond to calls must be trained and practised not only to direct
CPR but also nurses
to
deal with difficult situations. Both doctors and
require repeated, complete training.
Department of Clinical Pharmacology, and Department of Cardiology, University of Dundee, Nmewells Hospital, Dundee DD1 9SY
Combined with the issue of pocket masks to all trained personnel the above approach could greatly improve airway management in the vital first few minutes of cardiac or respiratory arrest and so improve the chances of a successful outcome. Department of Anaesthetics, Royal Berkshire Hospital, Reading, Berks RG1 5AN
P. H. SEIDELIN A. B. BRIDGES
DV, Camm AJ, Miles S. Cardiopulmonary resuscitation skills of preregistration house officers. Br Med J 1985; 290: 1549-50 2. Kaye W, Wynne G, Marteau T, Dubin HG, Rallis S, Evans TR. Evaluation of an advanced resuscitation training course for preregistration house officers Br Heart J 1. Skinner
1988; 59: 111. SR, Hansbrough JF, Libby LS, Hill DM, Mountain RD, Scoggin CH Cardiopulmonary resuscitation by medical and surgical house officers Lancet
3. Lowenstem
WILLIAM J. BRAMPTON
1981, ii: 679-81. PH, Stolarek IH, Littlewood DG Comparison of six methods of emergency ventilation. Lancet 1986, ii 1274-75.
4 Seidelm
D, Baran C. Ventilatory volumes using mouth-to-mouth, mouth-to-mask and bag valve mask techniques. Am J Emerg Med 1985; 3: 292. Jesudian MCS, Hanson RR, Keenan RL, et al. Bag-valve-mask ventilation: two rescuers are better than one—preliminary report Crit Care Med 1985; 13: 122
1. Hess 2.
PAINLESS LITHOTRIPSY
SiR,—Mr Philp and his colleagues (Jan 2/9, p 41) describe their
SiR,—Your Feb 6 editorial and the letter from Dr Lawler and colleagues raise several important issues about cardiopulmonary resuscitation (CPR) and training. Lawler et al state that there are no published reports of performance, by junior doctors in the UK, of advanced techniques. However, Skinner et aP have published a multiple choice questionnaire assessment of advanced technique and describe the poor performance of intubation (an advanced technique) by junior doctors, and Kaye et aF have assessed advanced cardiac life support in 60 newly qualified doctors. Lawler et al argue that training junior doctors raises formidable logistic problems; that junior doctors, because they move between wards, hospitals, and health districts, may not be familiar with the diverse equipment available; and that junior doctors may take part in a cardiac arrest only once every 3-5 days. All true but even more true for nurses or paramedical staff. For example, a nurse working a 371 hour week will attend about half as many arrests as a house-officer working 75-100 hours. Also house-officers usually attend cardiac arrests in more than one ward or even throughout a hospital. For an effective rapid response to a cardiac arrest there are two requirements-namely, the widespread location of advanced CPR equipment, preferably on every ward; and a trained person always present on the ward who will be responsible for starting basic and advanced resuscitation immediately. For the arrest trolley and arrive after the arrest team has assembled is a trained person on each shift and on every ward means that very large numbers must be trained. Since they will attend few arrests continuous retraining is essential. Retention of skills after training seems to be poor after 3-6 months.
defibrillator
to
unacceptable.
To have
with the Wolf Piezolith 2200. A similar machine was installed in Edinburgh last autumn, and we have treated 60 patients so far. We find it not only feasible but also highly desirable to treat patients on an outpatient basis. Apart from the obvious economic benefits, an outpatient visit lasting only 2 hours or so is preferred by most patients since it causes far less disruption than even one overnight stay, especially for patients in employment or mothers with young families. Over 75% of our patients received their first
experience
treatment as
outpatients.
The procedure is painless and was done without anaesthesia or sedation in all 60 patients. Only once was treatment foreshortened because of pain; we have also successfully treated 1 patient after incomplete therapy on another supposedly painless secondgeneration lithotripter when the patient had to be anaesthetised because she found the procedure too painful. Patients do require more treatments to render them stone-free than they do with first-generation machines but so far in our short experience no surgical intervention has been required before or after lithotripsy. 44 patients have had one lithotripsy session (of up to 4000 shocks); 15 cases became stone-free. 11patients have had two and 5 have had three sessions; 5 and 2, respectively, became stone-free. There appear to be differences in the stone-free rate of our patients compared with those treated by Philp et al (table). However, Philp and
colleagues do not say at what time patients are judged to be stone-free, and we treated a more complex group of stones-half our patients had either staghom or multiple calculi compared with a fifth in Philp et al’s series. In addition, we included 7 patients with ureteric
stones.
651 COMPARISON OF STONE-FREE RATES IN ALL PATIENTS WHO WERE TREATED WITH SECOND-GENERATION LITHOTRIPTER
(8) Increased intrathecal IgG synthesis was observed in HAM8 and has also been demonstrated in TSP.9 (9) HTLV-1 has been isolated from CSF lymphocytes in HAM 10 and TSP." (10) The neuropathological picture of HAM" and TSP" seems to
Our patients were evaluated at one month, when 37% were stone-free and fragmentation was apparent in a further 45 %, which gives an overall fragmentation rate of 82%. However, we believe that this does not give a true indication of stone clearance because patients will continue to pass fragments for up to 3 months. Though Philp and colleagues stress the requirement for repeat sessions and report the number of failures, they do not comment on the reason for failure. Can they be certain about accurate localisation? We recorded the ultrasound findings in every case and analysis of these data after apparent treatment failure showed that in 5 of the initial 20 patients the stone did not lie in the focus of the shock-wave. Most of these patients were successfully treated with a second session and our subsequent failure rate fell dramatically. Hence some of our early treatment "failures" were due to lack of operator experience with ultrasound localisation, although 6 failures did occur when the stone was located by ultrasound. These appear to be hard laminated stones, which generally occur in a small pelvicalyceal system and which did not fragment even after 7000
shocks. The present system of reporting results of lithotripsy has shortcomings, especially when mixed groups of patients are treated. The large number of second-generation lithotripters now on the market will inevitably lead to comparison of machine performance. The present descriptive accounts make such comparisons impossible and therefore, while there is no place for randomised clinical trials, there is an urgent need for urologists using new technology to standardise reporting. Commercial pressures may otherwise wrongly influence clinical judgment with obvious undesirable consequences. Scottish Lithotriptor Centre, Edinburgh EH3 9YW; and Royal Infirmary, Edinburgh
D. A. TOLLEY
be identical. On the basis of
our
personal experience
we
conclude that
HTLV-1-associated TSP and HAM are identical. Differences in early reports are probably explicable mainly by case-ascertainment bias; and the few differences that remain may be the result of genetic or other factors. Texas Tech University School of Medicine, Lubbock, Texas 79430, USA
GUSTAVO C. ROMÁN
Faculty of Medicine, Kagoshima University, Kagoshima, Japan
MITSUHIRO OSAME
1. Roman GC. The neuroepidemiology of tropical spastic paraparesis. Ann Neurol 1988,
23
(suppl): S113-S120. M, Igata A, Matsumoto M, Usuku K, Izumo S, Kosaka K HTLV-Iassociated myelopathy a report of 85 cases. Ann Neurol 1987; 22: 116 3. Vemant JC, Maurs L, Gessain A, et al. Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I: a clinical and seroepidemiological study of 25 cases Ann Neurol 1987; 21: 123-30. 4. Morgan OStC, Rodgers-Johnson P, Gibbs WN, Garruto RM, Gajdusek DC, Resnick L. Abnormal peripheral lymphocytes in tropical spastic paraparesis. Lancet 1987;
2. Osame
ii: 403-04. 5. Osame
M, Igata A, Matsumoto M, Usuku K, Kitajima I, Takahashi K. On the discovery of a new clinical entity: Human T-cell lymphotropic virus type I-associated myelopathy (HAM). Adv Neurol Sci ( Tokyo, Japan) 1987; 31:
727-45. 6. Tournier-Lasservé
E, Gout O, Gessain A, et al. HTLV-I, brain abnormalities on magnetic resonance imaging, and relation with multiple sclerosis. Lancet 1987, ii: 49-50 7. Vemant JC, Maurs L, Gout O, et al. HTLV-I-associated tropical spastic paraparesis in Martinique a reappraisal. Ann Neurol 1988; 23 (suppl): S133-S135. 8. Osame M, Usuku K, Izumo K, et al. HTLV-I-associated myelopathy: a new clinical entity Lancet 1986, i 1031-32 9. Ceroni M, Piccardo P, Rodgers-Johnson P, et al Intrathecal synthesis of IgG antibodies to HTLV-I supports an etiological role for HTLV-I in tropical spastic paraparesis. Ann Neurol 1988; 23 (suppl): S188-S191 10 Hirose S, Uemura Y, Fijishita M, et al Isolation of HTLV-I from cerebrospinal fluid of a patient with myelopathy. Lancet 1986; i: 397-98. 11. Akizuki S, Nakazato O, Higuchi Y, et al. Necropsy findings in HTLV-I-associated myelopathy. Lancet 1987; i. 156-57. 12. Piccardo P, Ceroni M, Rodgers-Johnson P, et al Pathological and immunological observations on tropical spastic paraparesis m patients from Jamaica. Ann Neurol 1988; 23 (suppl): S156-S160.
J. REID TETRACYCLINE-RESISTANT GONOCOCCI IN UK
IDENTITY OF HTLV-I-ASSOCIATED TROPICAL SPASTIC PARAPARESIS AND HTLV-I-ASSOCIATED MYELOPATHY
SIR,-As your Jan 30 editorial (p 217) points out tropical spastic paresis (TSP) and a myelopathy described in Japan (HAM) have been associated with human T-lymphotropic virus type 1 (HTLV-1). In early reports there were differences between the two conditions. Are they the same or not? One of us (G. C. R.) with experience of tropical myeloneuropathies, has now visited Kagoshima, Japan, to examine patients with HAM and compare them with HTLV-1 associated TSP patients from Colombia, the Seychelles, and the Caribbean. The following features were noted: (1) The geographical distribution of the two myelopathies follows that of HTLV-1 and adult T-cell leukaemia/lymphoma
(ATLL).’ (2) Clinical features, including age of onset, female preponderance, and pattern of onset and progression are similar,
including the occurrence of a mild thoracic level sensory deficit in a minority of cases of both HAM2 and TSP patients.3 (3) Only 36% of HAM cases have rare ATL-like cells in peripheral bloodand these cells have now been described in TSP.4 (4) The mild CSF pleocytosis reported in HAM’ has also been found in TSP.3
(5) Magnetic resonance imaging abnormalities in the brain of TSP patients6 have also been found in HAM.’* (6) Corticosteroid responsiveness has been reported in some HAM patients2 but in TSP a poor response is the norm.1 (7) In Kagoshima, 21 % of HAM blood transfusion2and TSP.7
a
similar
cases
history has
have had a history of now been reported in
SiR,—Plasmid-mediated, high-level tetracycline resistance (minimum inhibitory concentration [MIC] above 16 mg/1) was first recognised in Neisseria gonorrhoeae in the United States in February, 1985.1 Resistance is due to the insertion of the streptococcal tetM determinant into the 24megadalton (MD) gonococcal conjugative plasmid. This results in a plasmid of 25-2 MD.2 There have since been several reports of these tetracyclineresistant N gonorrhoeae (TRNG) in North America.3 The only examples in the UK, to our knowledge, are two strains isolated from homosexual men in Leeds, one of which originated in London (A. Jephcott, Gonococcus Reference Laboratory, personal communication). We have screened 1500 gonococcal isolates from patients attending the Praed Street Clinic since September, 1986, using media containing 10 mg/1 tetracycline. We have encountered 8 infections caused by TRNG, all isolated in 1988. All infections were from heterosexual patients, six men and two women, including two pairs of sexual contacts. For all strains the MIC was above 16 mg/1 for tetracycline, 0 25 mg/1 for penicillin, and 16-32 mg/1 for spectinomycin. All strains belonged to auxotype/serovar (A/S) class prototrophic IB-2. TRNG are of concern because the resistance determinant is present on the transmissible plasmid. In the United States evidence suggests dissemination of this plasmid amongst gonococci of different A/S classes.3 TRNG have been isolated from infections in’ both the heterosexual and homosexual population. In the UK tetracycline is rarely used for the treatment of gonorrhoea. However, the use of a tetracycline for the treatment of chlamydial
infections, including post-gonococcal urethritis, could selective pressure and hence aid the
spread
exert
of these strains.
SiR,—Your Feb 6th editorial emphasised the importance of
cardiopulmonary
resuscitation
training and retraining for hospital
staff. However, I agree with Dr Lawler and his colleagues (Feb 27, p 468) that the aim of all hospital doctors being able to intubate is logistically impossible. Semi-skilled intubation by the occasional practitioner in difficult conditions is, all too often, counterproductive, because it takes too long and may result in unrecognised oesophageal placement. As such it is an inappropriate method of immediate airway management. Unfortunately Lawler and colleagues’ further suggestion that the technical aspects of advanced arrest management, including intubation, should be delegated to suitably trained paramedical staff does not address the major problem of such immediate management. There is no reason to assume that a paramedical team will arrive any sooner than current arrest teams. Therefore all staff must be adequately trained in simple and effective airway management. Who actually intubates is unimportant provided they well trained, rapid, and skilful. An effective, simple, and hygienic technique for one-person ventilation is mouth-to-mask, preferably with supplemental oxygen. This method is easily learned and retained, and should be taught in preference to a bag-valve-mask technique, which is a difficult method for one person to master and should therefore be taught as the more effective two-person technique.2 Cricoid pressure is an important adjunct to these methods and should receive more emphasis. Intubation training and retraining should be provided for senior members of the cardiac arrest team and of the intensive care unit and for designated accident and emergency are
personnel.
Semiautomatic defibrillators may be helpful. Intubation requires repeated practice, which, for the training of large numbers, cannot and should not be on patients. We find mannikins to be essential for such training. We, like others, have found that the use of mannikins for full simulated cardiac arrests and intubation induces anxiety, and junior doctors feel that these simulations help them to cope better with true cardiac arrest, allowing them to concentrate on difficulties. Thus the "sheer terror of intubating a cyanosed patient whose mouth is full of secretions" is replaced, with practice, by the ability to see such a patient as one with a major complication to be approached calmly and efficiently using well-rehearsed techniques. We agree that for the apnoeic patient the ideal is for rapid, skilled intubation. Where such skills are not available pocket masks with exhaled air ventilation and supplemental oxygen are superior to incompetent intubation attempts, inadequate "ambu" bagging, Brook airway, or exhaled air ventilation alone.’ Training in the use of pocket masks can be easily incorporated into a hospital’s basic life-support training programme. The answer to the question "CPR: whose job?" is that CPR remains a team response. Hospitals must ensure that there are enough defibrillators to permit the response to an arrest call to be rapid, and we should start to standardise the equipment provided. Someone able to defibrillate must be on the spot. An appropriate protocol for airway management should be arrived at.’ Those who respond to calls must be trained and practised not only to direct
CPR but also nurses
to
deal with difficult situations. Both doctors and
require repeated, complete training.
Department of Clinical Pharmacology, and Department of Cardiology, University of Dundee, Nmewells Hospital, Dundee DD1 9SY
Combined with the issue of pocket masks to all trained personnel the above approach could greatly improve airway management in the vital first few minutes of cardiac or respiratory arrest and so improve the chances of a successful outcome. Department of Anaesthetics, Royal Berkshire Hospital, Reading, Berks RG1 5AN
P. H. SEIDELIN A. B. BRIDGES
DV, Camm AJ, Miles S. Cardiopulmonary resuscitation skills of preregistration house officers. Br Med J 1985; 290: 1549-50 2. Kaye W, Wynne G, Marteau T, Dubin HG, Rallis S, Evans TR. Evaluation of an advanced resuscitation training course for preregistration house officers Br Heart J 1. Skinner
1988; 59: 111. SR, Hansbrough JF, Libby LS, Hill DM, Mountain RD, Scoggin CH Cardiopulmonary resuscitation by medical and surgical house officers Lancet
3. Lowenstem
WILLIAM J. BRAMPTON
1981, ii: 679-81. PH, Stolarek IH, Littlewood DG Comparison of six methods of emergency ventilation. Lancet 1986, ii 1274-75.
4 Seidelm
D, Baran C. Ventilatory volumes using mouth-to-mouth, mouth-to-mask and bag valve mask techniques. Am J Emerg Med 1985; 3: 292. Jesudian MCS, Hanson RR, Keenan RL, et al. Bag-valve-mask ventilation: two rescuers are better than one—preliminary report Crit Care Med 1985; 13: 122
1. Hess 2.
PAINLESS LITHOTRIPSY
SiR,—Mr Philp and his colleagues (Jan 2/9, p 41) describe their
SiR,—Your Feb 6 editorial and the letter from Dr Lawler and colleagues raise several important issues about cardiopulmonary resuscitation (CPR) and training. Lawler et al state that there are no published reports of performance, by junior doctors in the UK, of advanced techniques. However, Skinner et aP have published a multiple choice questionnaire assessment of advanced technique and describe the poor performance of intubation (an advanced technique) by junior doctors, and Kaye et aF have assessed advanced cardiac life support in 60 newly qualified doctors. Lawler et al argue that training junior doctors raises formidable logistic problems; that junior doctors, because they move between wards, hospitals, and health districts, may not be familiar with the diverse equipment available; and that junior doctors may take part in a cardiac arrest only once every 3-5 days. All true but even more true for nurses or paramedical staff. For example, a nurse working a 371 hour week will attend about half as many arrests as a house-officer working 75-100 hours. Also house-officers usually attend cardiac arrests in more than one ward or even throughout a hospital. For an effective rapid response to a cardiac arrest there are two requirements-namely, the widespread location of advanced CPR equipment, preferably on every ward; and a trained person always present on the ward who will be responsible for starting basic and advanced resuscitation immediately. For the arrest trolley and arrive after the arrest team has assembled is a trained person on each shift and on every ward means that very large numbers must be trained. Since they will attend few arrests continuous retraining is essential. Retention of skills after training seems to be poor after 3-6 months.
defibrillator
to
unacceptable.
To have
with the Wolf Piezolith 2200. A similar machine was installed in Edinburgh last autumn, and we have treated 60 patients so far. We find it not only feasible but also highly desirable to treat patients on an outpatient basis. Apart from the obvious economic benefits, an outpatient visit lasting only 2 hours or so is preferred by most patients since it causes far less disruption than even one overnight stay, especially for patients in employment or mothers with young families. Over 75% of our patients received their first
experience
treatment as
outpatients.
The procedure is painless and was done without anaesthesia or sedation in all 60 patients. Only once was treatment foreshortened because of pain; we have also successfully treated 1 patient after incomplete therapy on another supposedly painless secondgeneration lithotripter when the patient had to be anaesthetised because she found the procedure too painful. Patients do require more treatments to render them stone-free than they do with first-generation machines but so far in our short experience no surgical intervention has been required before or after lithotripsy. 44 patients have had one lithotripsy session (of up to 4000 shocks); 15 cases became stone-free. 11patients have had two and 5 have had three sessions; 5 and 2, respectively, became stone-free. There appear to be differences in the stone-free rate of our patients compared with those treated by Philp et al (table). However, Philp and
colleagues do not say at what time patients are judged to be stone-free, and we treated a more complex group of stones-half our patients had either staghom or multiple calculi compared with a fifth in Philp et al’s series. In addition, we included 7 patients with ureteric
stones.
651 COMPARISON OF STONE-FREE RATES IN ALL PATIENTS WHO WERE TREATED WITH SECOND-GENERATION LITHOTRIPTER
(8) Increased intrathecal IgG synthesis was observed in HAM8 and has also been demonstrated in TSP.9 (9) HTLV-1 has been isolated from CSF lymphocytes in HAM 10 and TSP." (10) The neuropathological picture of HAM" and TSP" seems to
Our patients were evaluated at one month, when 37% were stone-free and fragmentation was apparent in a further 45 %, which gives an overall fragmentation rate of 82%. However, we believe that this does not give a true indication of stone clearance because patients will continue to pass fragments for up to 3 months. Though Philp and colleagues stress the requirement for repeat sessions and report the number of failures, they do not comment on the reason for failure. Can they be certain about accurate localisation? We recorded the ultrasound findings in every case and analysis of these data after apparent treatment failure showed that in 5 of the initial 20 patients the stone did not lie in the focus of the shock-wave. Most of these patients were successfully treated with a second session and our subsequent failure rate fell dramatically. Hence some of our early treatment "failures" were due to lack of operator experience with ultrasound localisation, although 6 failures did occur when the stone was located by ultrasound. These appear to be hard laminated stones, which generally occur in a small pelvicalyceal system and which did not fragment even after 7000
shocks. The present system of reporting results of lithotripsy has shortcomings, especially when mixed groups of patients are treated. The large number of second-generation lithotripters now on the market will inevitably lead to comparison of machine performance. The present descriptive accounts make such comparisons impossible and therefore, while there is no place for randomised clinical trials, there is an urgent need for urologists using new technology to standardise reporting. Commercial pressures may otherwise wrongly influence clinical judgment with obvious undesirable consequences. Scottish Lithotriptor Centre, Edinburgh EH3 9YW; and Royal Infirmary, Edinburgh
D. A. TOLLEY
be identical. On the basis of
our
personal experience
we
conclude that
HTLV-1-associated TSP and HAM are identical. Differences in early reports are probably explicable mainly by case-ascertainment bias; and the few differences that remain may be the result of genetic or other factors. Texas Tech University School of Medicine, Lubbock, Texas 79430, USA
GUSTAVO C. ROMÁN
Faculty of Medicine, Kagoshima University, Kagoshima, Japan
MITSUHIRO OSAME
1. Roman GC. The neuroepidemiology of tropical spastic paraparesis. Ann Neurol 1988,
23
(suppl): S113-S120. M, Igata A, Matsumoto M, Usuku K, Izumo S, Kosaka K HTLV-Iassociated myelopathy a report of 85 cases. Ann Neurol 1987; 22: 116 3. Vemant JC, Maurs L, Gessain A, et al. Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I: a clinical and seroepidemiological study of 25 cases Ann Neurol 1987; 21: 123-30. 4. Morgan OStC, Rodgers-Johnson P, Gibbs WN, Garruto RM, Gajdusek DC, Resnick L. Abnormal peripheral lymphocytes in tropical spastic paraparesis. Lancet 1987;
2. Osame
ii: 403-04. 5. Osame
M, Igata A, Matsumoto M, Usuku K, Kitajima I, Takahashi K. On the discovery of a new clinical entity: Human T-cell lymphotropic virus type I-associated myelopathy (HAM). Adv Neurol Sci ( Tokyo, Japan) 1987; 31:
727-45. 6. Tournier-Lasservé
E, Gout O, Gessain A, et al. HTLV-I, brain abnormalities on magnetic resonance imaging, and relation with multiple sclerosis. Lancet 1987, ii: 49-50 7. Vemant JC, Maurs L, Gout O, et al. HTLV-I-associated tropical spastic paraparesis in Martinique a reappraisal. Ann Neurol 1988; 23 (suppl): S133-S135. 8. Osame M, Usuku K, Izumo K, et al. HTLV-I-associated myelopathy: a new clinical entity Lancet 1986, i 1031-32 9. Ceroni M, Piccardo P, Rodgers-Johnson P, et al Intrathecal synthesis of IgG antibodies to HTLV-I supports an etiological role for HTLV-I in tropical spastic paraparesis. Ann Neurol 1988; 23 (suppl): S188-S191 10 Hirose S, Uemura Y, Fijishita M, et al Isolation of HTLV-I from cerebrospinal fluid of a patient with myelopathy. Lancet 1986; i: 397-98. 11. Akizuki S, Nakazato O, Higuchi Y, et al. Necropsy findings in HTLV-I-associated myelopathy. Lancet 1987; i. 156-57. 12. Piccardo P, Ceroni M, Rodgers-Johnson P, et al Pathological and immunological observations on tropical spastic paraparesis m patients from Jamaica. Ann Neurol 1988; 23 (suppl): S156-S160.
J. REID TETRACYCLINE-RESISTANT GONOCOCCI IN UK
IDENTITY OF HTLV-I-ASSOCIATED TROPICAL SPASTIC PARAPARESIS AND HTLV-I-ASSOCIATED MYELOPATHY
SIR,-As your Jan 30 editorial (p 217) points out tropical spastic paresis (TSP) and a myelopathy described in Japan (HAM) have been associated with human T-lymphotropic virus type 1 (HTLV-1). In early reports there were differences between the two conditions. Are they the same or not? One of us (G. C. R.) with experience of tropical myeloneuropathies, has now visited Kagoshima, Japan, to examine patients with HAM and compare them with HTLV-1 associated TSP patients from Colombia, the Seychelles, and the Caribbean. The following features were noted: (1) The geographical distribution of the two myelopathies follows that of HTLV-1 and adult T-cell leukaemia/lymphoma
(ATLL).’ (2) Clinical features, including age of onset, female preponderance, and pattern of onset and progression are similar,
including the occurrence of a mild thoracic level sensory deficit in a minority of cases of both HAM2 and TSP patients.3 (3) Only 36% of HAM cases have rare ATL-like cells in peripheral bloodand these cells have now been described in TSP.4 (4) The mild CSF pleocytosis reported in HAM’ has also been found in TSP.3
(5) Magnetic resonance imaging abnormalities in the brain of TSP patients6 have also been found in HAM.’* (6) Corticosteroid responsiveness has been reported in some HAM patients2 but in TSP a poor response is the norm.1 (7) In Kagoshima, 21 % of HAM blood transfusion2and TSP.7
a
similar
cases
history has
have had a history of now been reported in
SiR,—Plasmid-mediated, high-level tetracycline resistance (minimum inhibitory concentration [MIC] above 16 mg/1) was first recognised in Neisseria gonorrhoeae in the United States in February, 1985.1 Resistance is due to the insertion of the streptococcal tetM determinant into the 24megadalton (MD) gonococcal conjugative plasmid. This results in a plasmid of 25-2 MD.2 There have since been several reports of these tetracyclineresistant N gonorrhoeae (TRNG) in North America.3 The only examples in the UK, to our knowledge, are two strains isolated from homosexual men in Leeds, one of which originated in London (A. Jephcott, Gonococcus Reference Laboratory, personal communication). We have screened 1500 gonococcal isolates from patients attending the Praed Street Clinic since September, 1986, using media containing 10 mg/1 tetracycline. We have encountered 8 infections caused by TRNG, all isolated in 1988. All infections were from heterosexual patients, six men and two women, including two pairs of sexual contacts. For all strains the MIC was above 16 mg/1 for tetracycline, 0 25 mg/1 for penicillin, and 16-32 mg/1 for spectinomycin. All strains belonged to auxotype/serovar (A/S) class prototrophic IB-2. TRNG are of concern because the resistance determinant is present on the transmissible plasmid. In the United States evidence suggests dissemination of this plasmid amongst gonococci of different A/S classes.3 TRNG have been isolated from infections in’ both the heterosexual and homosexual population. In the UK tetracycline is rarely used for the treatment of gonorrhoea. However, the use of a tetracycline for the treatment of chlamydial
infections, including post-gonococcal urethritis, could selective pressure and hence aid the
spread
exert
of these strains.